Fig. 4From: Decoding the synaptic dysfunction of bioactive human AD brain soluble Aβ to inspire novel therapeutic avenues for Alzheimer’s diseaseSoluble Aβ oligomers from other sources also inhibit hippocampal LTP. Several sources of soluble Aβ included (a) AD patient CSF; (b) APP tg mouse of AD (J20 mice); (c) cell secreted human soluble Aβ; and (d) synthetic Aβ1–42 peptide, effect on hippocampal LTP. All these impaired hippocampal LTP (red), while the inhibition of LTP by the 3 biological sources was prevented by removing soluble Aβ via immunodepletion (blue)Back to article page